Osmotic forces are not critical for Ca 2+ -induced secretion from permeabilized human neutrophils

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dc.contributor.author Stoehr, Sally Jo en_US
dc.contributor.author Smolen, James E. en_US
dc.date.accessioned 2007-04-06T18:03:56Z
dc.date.available 2007-04-06T18:03:56Z
dc.date.issued 1988-05 en_US
dc.identifier.citation Stoehr, Sally Jo; Smolen, James E. (1988)."Osmotic forces are not critical for Ca 2+ -induced secretion from permeabilized human neutrophils." Journal of Cellular Physiology 135(2): 169-178. <http://hdl.handle.net/2027.42/49877> en_US
dc.identifier.issn 0021-9541 en_US
dc.identifier.issn 1097-4652 en_US
dc.identifier.uri http://hdl.handle.net/2027.42/49877
dc.identifier.uri http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=3372594&dopt=citation en_US
dc.description.abstract In order to examine the role of osmotic forces in degranulation, the effects of solutes and osmolality on granule secretion were explored using both FMLP-stimulated, intact neutrophils and Ca 2+ -stimulated, permeabilized cells. We employed a HEPES-based buffer system which was supplemented with: (a) permeant (KCl or NaCI) or impermeant (Na-isethionate or choline-CI) ions, or (b) permeant (urea) or impermeant (sucrose) uncharged solutes. Intact and permeabilized cells had significantly different solute requirements for degranulation. FMLP-stimulated release from intact cells was supported by NaCI or Na-isethionate > KCl > choline-Cl or sucrose > urea. In contrast, the rank order of Ca 2+ -stimulated release from permeabilized cells was choline-C > Na-isethionate, KCl, or NaCl > sucrose > urea. Hypo-osmotic conditions caused increased levels of background granule release from both intact and permeabilized neutrophils. However, hypo-osmolality inhibited both FMLP-stimulated degranulation from intact cells and Ca 2+ -induced release from permeabilized neutrophils. While hyperosmotic conditions inhibited stimulated release from intact cells, this inhibition was much less pronounced in permeabilized cells when the granules were directly exposed to these solutions. In fact, hyperosmotic sucrose greatly enhanced Ca 2+ -induced secretion. Although isolated specific and azurophil granules showed some lytic tendencies in hypo-osmotic buffers, the overall stability of the isolated granules did not indicate that swelling alone could effect degranulation. These results suggest that degranulation in permeabilized cells is neither due to nor driven by simple osmotic forces (under resting or stimulated conditions) and emphasize differences obtained by bathing both the granules and plasma membrane (as opposed to membranes alone) in various solutes. en_US
dc.format.extent 973912 bytes
dc.format.extent 3118 bytes
dc.format.mimetype application/pdf
dc.format.mimetype text/plain
dc.publisher Wiley Subscription Services, Inc., A Wiley Company en_US
dc.subject.other Life and Medical Sciences en_US
dc.subject.other Cell & Developmental Biology en_US
dc.title Osmotic forces are not critical for Ca 2+ -induced secretion from permeabilized human neutrophils en_US
dc.type Article en_US
dc.rights.robots IndexNoFollow en_US
dc.subject.hlbsecondlevel Molecular, Cellular and Developmental Biology en_US
dc.subject.hlbsecondlevel Kinesiology and Sports en_US
dc.subject.hlbtoplevel Health Sciences en_US
dc.subject.hlbtoplevel Science en_US
dc.description.peerreviewed Peer Reviewed en_US
dc.contributor.affiliationum Department of Pediatric Hematology-Oncology, The University of Michigan Medical Center, Ann Arbor, Michigan 48109 en_US
dc.contributor.affiliationum Department of Pediatric Hematology-Oncology, The University of Michigan Medical Center, Ann Arbor, Michigan 48109 ; Department of Pathology, The University of Michigan Medical Center, Ann Arbor, Michigan 48109 ; Department of Pediatric Hematology-Oncology, The University of Michigan Medical Center, Ann Arbor, Michigan 48109 en_US
dc.identifier.pmid 3372594 en_US
dc.description.bitstreamurl http://deepblue.lib.umich.edu/bitstream/2027.42/49877/1/1041350204_ftp.pdf en_US
dc.identifier.doi http://dx.doi.org/10.1002/jcp.1041350204 en_US
dc.identifier.source Journal of Cellular Physiology en_US
dc.owningcollname Interdisciplinary and Peer-Reviewed
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